The relaxin/insulin-like gene family includes signaling molecules that perform a variety of physiological roles mostly related to reproduction and neuroendocrine regulation. Several previous studies have focused on the evolutionary history of relaxin genes in anthropoid primates, with particular attention on resolving the duplication history of RLN1 and RLN2 genes, which are found as duplicates only in apes. These studies have revealed that the RLN1 and RLN2 paralogs in apes have a more complex history than their phyletic distribution would suggest. In this regard, alternative scenarios have been proposed to explain the timing of duplication, and the history of gene gain and loss along the organismal tree. In this article, we revisit the question and specifically reconstruct phylogenies based on coding and noncoding sequence in anthropoid primates to readdress the timing of the duplication event giving rise to RLN1 and RLN2 in apes. Results from our phylogenetic analyses based on noncoding sequence revealed that the duplication event that gave rise to the RLN1 and RLN2 occurred in the last common ancestor of catarrhine primates, between ∼ 44.2 and 29.6 Ma, and not in the last common ancestor of apes or anthropoids, as previously suggested. Comparative analyses based on coding and noncoding sequence suggests an event of convergent evolution at the sequence level between co-ortholog genes, the single-copy RLN gene found in New World monkeys and the RLN1 gene of apes, where changes in a fraction of the convergent sites appear to be driven by positive selection.
Keywords: convergent evolution; differential gene retention; gene duplication; positive selection; relaxin.